应用改良型ＴＮＦα（ＩＴＮＦα）和ＩＦＮγ刺激小鼠腹腔巨噬细胞（ＭΦ）诱生一氧化氮（ＮＯ），并观察对细胞毒作用的影响。结果：ＩＦＮγ可激活小鼠腹腔ＭΦ产生小量ＮＯ，并伴随产生低度细胞毒活性，尤其是对经ＩＦＮγ处理的靶细胞（γＬ１２１０细胞）为显著。单用ＩＴＮＦα刺激的ＭΦ，诱生ＮＯ不显著或微量，对靶细胞也无明显细胞毒作用。但ＩＴＮＦα（１００ｎｇ／ｍｌ）和ＩＦＮγ（５０Ｕ／ｍｌ）共同刺激ＭΦ，可产生有意义量的ＮＯ（Ｐ＜００５），对γＬ１２１０细胞有显著细胞作用（Ｐ＜００１），而对未经ＩＦＮγ处理的靶细胞（Ｌ１２１０ｃｅｌｓ）无明显细胞毒作用。这可能是ＩＦＮγ促进ＭΦ诱生ＮＯ和靶细胞表面粘附分子的表达，加强效靶识别和结合，提高了对靶细胞的杀伤力。 Ischemia peritoneal macrophages (MΦ) were used to induce nitric oxide (NO) by modified TNFα and IFNγ, and the effects on cytotoxicity were observed. RESULTS: IFN-γ could activate MΦ in mice’s peritoneal cavity to produce a small amount of NO, with concomitant low cytotoxic activity, especially for IFN-γ-treated target cells (γ-L1210 cells). MΦ stimulated with I  TNF  α alone did not induce significant or trace NO, and had no significant cytotoxic effect on target cells. However, TNF-α (100 ng/ml) and IFN-γ (50 U/ml) co-stimulated MΦ, which could produce a significant amount of NO (P<005), and had a significant cellular effect on γL1210 cells (P <001), but no significant cytotoxicity to target cells (L1210cels) that have not been treated with IFN-γ. This may be due to the fact that IFN-γ promotes MΦ-induced NO and the expression of adhesion molecules on the target cell surface, enhances target recognition and binding, and increases the lethality to target cells.